Asthma and chronic obstructive pulmonary disease (COPD) are diseases affecting the respiratory system, which millions of people suffer from. These diseases are today regarded as inflammatory diseases and the symptoms comprise constriction of the airways. Common treatment of the associated bronchoconstriction involves use of beta-agonists, such as terbutalin and formoterol, and anticholinergics, such as ipratropium bromide and tiotropium bromide.
Hypertension, i.e. high blood pressure, increases the risk of stroke, heart attacks, heart failure and kidney disease. Medications presently used for the treatment of hypertension include the administration of beta-blockers, calcium channel blockers, diuretics, angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists. Vasoconstriction results in an increase in the blood pressure.
The treatments for prevention, revocation or reduction of bronchoconstricion and vasoconstriction are in many ways insufficient and there is a need for alternative treatments.
More specifically, there is a need of compounds also being effective in preventing or revoking bronchoconstriction within the small airways, such as human airways having a diameter of less than 2.0 mm. It is believed that a bronchodilating effect on small airways (noncartilaginous airways of 2.0 mm or less in inner diameter) is of greater relevance for clinically observed relief of symptoms in COPD (i.e. shortness of breath), and maybe even in severe asthma, as compared to bronchodilation of larger bronchi (more than 2 mm in inner diameter), due to the greater total surface area associated with the former.
Furthermore, there is a need for compounds being effective in preventing or revoking bronchoconstriction, whose mechanisms differs from pharmacological established mechanisms of bronchodilation and preferably being effective in preventing or revoking bronchoconstriction within the small airways. Accordingly, there is a need for compounds being effective in preventing or revoking bronchoconstriction and which neither affect adrenergic or muscarinic receptors nor increasing the levels of cAMP through inhibition of phosphodiesterase enzymes, such as PDE3A enzyme.